Family history of essential hypertension versus obesity as risk factors for hypertension in adolescents

Abstract

Family history of hypertension and obesity are both risk factors for hypertension. Hypertension and obesity share several physiopathologic abnormalities and are frequently associated. However, not all obese people are hypertensive. Renal handling of sodium has been proposed as a physiopathogenic mechanism of essential hypertension and obesity. This study was conducted in obese adolescents to evaluate the role of a family history of hypertension versus obesity in the renal handling of sodium. Fractional excretion of lithium (FELi) and uric acid (FEUA) were measured in 46 obese adolescent offspring of hypertensive parents (OH: body mass index [BMI], 29.5 ± 0.6 kg/m 2, age 14.2 ± 0.3 years, 22 males); eight obese offspring of normotensive parents (ON: BMI, 30.7 ± 1.7 kg/m 2, 14.8 ± 0.8 years, four males), and in 34 lean adolescent offspring of hypertensive parents (LH: BMI, 20.5 ± 0.5 kg/m 2, 14.3 ± 0.3 years, 24 males). FELi in OH was 16.5% ± 1.3%, in ON it was 22.4% ± 2.3%, and in LH it was 14.4% ± 1.2% ( P < .05). FEUA in OH was 8.5% ± 0.8%, in ON it was 14.8% ± 3.6%, and in LH it was 7.9% ± 0.8% ( P < .01). Plasma renin activity (PRA) and aldosterone (PA) were measured in OH and LH; PRA was 5.3 ± 0.4 and 4.5 ± 0.4 ng/mL/h, respectively ( P = NS), and PA was 366 ± 36 and 242 ± 32 pg/mL, respectively ( P < .05). In summary, adolescents with a family history of hypertension, regardless of their body mass, have a diminished FELi and FEUA. Obese adolescents also have higher plasma levels of aldosterone than lean ones. In conclusion, the family history of hypertension would be related to the increased renal proximal sodium reabsorption whereas obesity would be related to increased distal sodium reabsorption mechanisms, such as aldosterone. Both mechanisms could explain the higher prevalence of hypertension in obese offspring of hypertensive parents.